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ST-SEGMENT DEPRESSION IN LEAD AVR PREDICTS 30-DAY ADVERSE OUTCOMES IN PATIENTS WITH INFERIOR ACUTE MYOCARDIAL INFARCTION
475 JACC April 5, 2016 Volume 67, Issue 13
Acute Coronary Syndromes ST-SEGMENT DEPRESSION IN LEAD AVR PREDICTS 30-DAY ADVERSE OUTCOMES IN PATIENTS WITH INFERIOR ACUTE MYOCARDIAL INFARCTION Poster Contributions Poster Area, South Hall A1 Saturday, April 02, 2016, 10:00 a.m.-10:45 a.m. Session Title: Predicting Outcomes in Acute Coronary Syndromes Abstract Category: 14. Acute Coronary Syndromes: Clinical Presentation Number: 1100-003 Authors: Masami Kosuge, Toshiaki Ebina, Kiyoshi Hibi, Kengo Tsukahara, Noriaki Iwahashi, Nobuhiko Maejima, Eiichi Akiyama, Satoshi Umemura, Kazuo Kimura, Yokohama City University Medical Center, Yokohama, Japan Background: During inferior acute myocardial infarction (IMI), ST-segment depression in lead aVR (ST↓aVR) can be caused by a reciprocal change of ST-segment elevation in lead -aVR facing the apical wall, suggesting a larger area at risk. We examined the prognostic implication of ST↓aVR in patients with reperfused IMI.
Methods: We studied 377 patients with a first IMI who underwent reperfusion therapy and had TIMI 3 flow within 6 h after symptom onset. Patients were divided into the 3 groups according to the degree of ST↓aVR on admission ECG: group A, 174 patients with no ST↓aVR; group B, 134 patients with ST↓aVR ≤1.0 mm; and group C, 69 patients with ST↓aVR >1.0 mm. The perfusion territory of the culprit artery was assessed on the basis of the angiographic distribution score. Impaired myocardial reperfusion was defined as myocardial blush grade 0/1 on the final angiogram. Results: There were no differences in age, sex, coronary risk factors, time from symptom onset to admission, culprit artery (the right coronary artery or left circumflex coronary artery), initial TIMI flow grade, reperfusion therapy or time to reperfusion among the 3 groups. In groups A, B, and C, the sum of ST-segment elevation in leads II, III, aVF and V5-6 on admission ECG was 4±4, 8±5, and 16±7 mm (p<0.01); the angiographic distribution score was 0.5±0.2, 0.6±0.2, and 0.7±0.1 (p<0.01); peak creatine kinase level was 2098±1444, 2866±1831, and 4656±2132 IU/L (p<0.01); and the rates of Killip class ≥2 on admission were 3%, 6%, and 12% (p=0.05); impaired myocardial reperfusion were 6%, 17%, and 64% (p<0.01); the combined outcomes of death, reinfarction, or heart failure at 30 days was 1%, 8%, and 19% (p<0.01), respectively. Multivariate analysis showed that as compared with no ST↓aVR, the hazard ratios (95%CI) for 30-day adverse events associated with ST↓aVR ≤1.0 mm and ST↓aVR >1.0 mm were 1.36 (0.84-3.69; p=0.14) and 2.70 (1.19-5.09; p<0.01), respectively.
Conclusions: In patients with reperfused IMI, greater ST↓aVR on admission ECG is associated with a larger area at risk, impaired myocardial reperfusion, and a larger infarct size. ST↓aVR >1.0 mm is a significant and independent predictor of 30-day adverse outcomes.
Acute Coronary Syndromes ST-SEGMENT DEPRESSION IN LEAD AVR PREDICTS 30-DAY ADVERSE OUTCOMES IN PATIENTS WITH INFERIOR ACUTE MYOCARDIAL INFARCTION Poster Contributions Poster Area, South Hall A1 Saturday, April 02, 2016, 10:00 a.m.-10:45 a.m. Session Title: Predicting Outcomes in Acute Coronary Syndromes Abstract Category: 14. Acute Coronary Syndromes: Clinical Presentation Number: 1100-003 Authors: Masami Kosuge, Toshiaki Ebina, Kiyoshi Hibi, Kengo Tsukahara, Noriaki Iwahashi, Nobuhiko Maejima, Eiichi Akiyama, Satoshi Umemura, Kazuo Kimura, Yokohama City University Medical Center, Yokohama, Japan Background: During inferior acute myocardial infarction (IMI), ST-segment depression in lead aVR (ST↓aVR) can be caused by a reciprocal change of ST-segment elevation in lead -aVR facing the apical wall, suggesting a larger area at risk. We examined the prognostic implication of ST↓aVR in patients with reperfused IMI.
Methods: We studied 377 patients with a first IMI who underwent reperfusion therapy and had TIMI 3 flow within 6 h after symptom onset. Patients were divided into the 3 groups according to the degree of ST↓aVR on admission ECG: group A, 174 patients with no ST↓aVR; group B, 134 patients with ST↓aVR ≤1.0 mm; and group C, 69 patients with ST↓aVR >1.0 mm. The perfusion territory of the culprit artery was assessed on the basis of the angiographic distribution score. Impaired myocardial reperfusion was defined as myocardial blush grade 0/1 on the final angiogram. Results: There were no differences in age, sex, coronary risk factors, time from symptom onset to admission, culprit artery (the right coronary artery or left circumflex coronary artery), initial TIMI flow grade, reperfusion therapy or time to reperfusion among the 3 groups. In groups A, B, and C, the sum of ST-segment elevation in leads II, III, aVF and V5-6 on admission ECG was 4±4, 8±5, and 16±7 mm (p<0.01); the angiographic distribution score was 0.5±0.2, 0.6±0.2, and 0.7±0.1 (p<0.01); peak creatine kinase level was 2098±1444, 2866±1831, and 4656±2132 IU/L (p<0.01); and the rates of Killip class ≥2 on admission were 3%, 6%, and 12% (p=0.05); impaired myocardial reperfusion were 6%, 17%, and 64% (p<0.01); the combined outcomes of death, reinfarction, or heart failure at 30 days was 1%, 8%, and 19% (p<0.01), respectively. Multivariate analysis showed that as compared with no ST↓aVR, the hazard ratios (95%CI) for 30-day adverse events associated with ST↓aVR ≤1.0 mm and ST↓aVR >1.0 mm were 1.36 (0.84-3.69; p=0.14) and 2.70 (1.19-5.09; p<0.01), respectively.
Conclusions: In patients with reperfused IMI, greater ST↓aVR on admission ECG is associated with a larger area at risk, impaired myocardial reperfusion, and a larger infarct size. ST↓aVR >1.0 mm is a significant and independent predictor of 30-day adverse outcomes.